Psychiatry Research 110 (2002) 201–217

Research on psychiatric outcomes and interventions subsequent to disasters: a review of the literature Craig L. Katza,b,*, Lori Pellegrinoa, Anand Pandyab,c, Anthony Ngb,c, Lynn E. DeLisib,c a

Department of Psychiatry, Mount Sinai School of Medicine, One Gustave L. Levy Place, Box 1230, New York, NY 10029-6574, USA b Disaster Psychiatry Outreach, New York, NY, USA c Department of Psychiatry, New York University, New York, NY, USA Received 20 November 2001; received in revised form 5 April 2002; accepted 17 April 2002

Abstract Tragic events such as those of September 11, 2001, underscore the increasingly prominent role that psychiatrists play in aiding survivors, emergency workers, and broader communities to cope with disaster. The present review was undertaken to identify whether there exists a scientific basis for the practice of psychiatry in the aftermath of disasters. Most of the extensive literature over the past 30 years suggests that disasters have psychopathological consequences as well as medical and social ones. Pre-existing mood and anxiety disorders, although surprisingly not psychotic illness, appear to be risk factors for further psychopathology after a disaster. Thus, both acute psychopharmacological and psychotherapeutic interventions at disaster sites may prevent long-term sequelae, although their efficacy remains uncertain. Future controlled treatment trials are needed to determine the optimal treatment strategy. 䊚 2002 Elsevier Science Ireland Ltd. All rights reserved. Keywords: Trauma; Emergency; Posttraumatic stress disorder; Acute intervention

1. Introduction Disasters are traumatic events that affect whole communities of individuals and cause widespread destruction and distress, unlike traumatic events that are understood to happen at the level of the individual (American Heritage Dictionary, 1982). Whether disasters are experienced as a psychosocial disruption (World Health Organization, 1992), *Corresponding author. Tel.: q1-212-659-8733; fax: q1212-659-9290. E-mail address: [email protected] (C.L. Katz).

a physical threat, or a massive psychological stress, mental health professionals have been increasingly called upon to assist during these acute crises (Kinston and Rosser, 1974). The recent events of September 11, 2001, underscored this, as it was sadly recognized over the coming days that the most important physicians to head the recovery efforts were psychiatrists, not emergency-trained trauma surgeons or internists (Lagnado, 2001). Disasters deserve special attention among human traumas for several reasons. They are distinguished by their magnitude and seeming capacity to traumatize a great many individuals at once.

0165-1781/02/$ - see front matter 䊚 2002 Elsevier Science Ireland Ltd. All rights reserved. PII: S 0 1 6 5 - 1 7 8 1 Ž 0 2 . 0 0 1 1 0 - 5

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Moreover, by definition, they overwhelm the social and political fabric of communities, a disruption that can be expected to significantly exacerbate and color individuals’ suffering in response to the trauma. Finally, disasters are the most public of traumas and thus offer unique opportunities to study human response to tragedy on any level. That psychiatrists and other mental health professionals have come to constitute an increasingly regular component of disaster response has led us to inquire into the empiric basis of such a practice. We therefore conducted a literature review dating to 1966 in order to establish what research has uncovered about the association of treatable psychiatric syndromes with disasters and about specific therapeutic interventions for these problems. The review concentrates on interventions that are available for purposes of either prevention or treatment during the acute period of a disaster, which we are defining as either the first 2 months after the event (based on the DSM-IV duration qualifiers for acute stress disorder) or the period during which the event continues to pose an immediate threat (i.e. while aftershocks continue after an earthquake). 2. Epidemiology of psychiatric symptoms and disorders A considerable number of psychiatric surveys have been conducted subsequent to earthquakes, hurricanes, volcanoes and various man-made disasters and document a range of psychiatric symptoms and disorders associated with these events (Tables 1 and 2). Rubonis and Bickman (1991) conducted a statistical review of studies that quantified psychopathology in the aftermath of disasters dating back to 1966 and, on the basis of this analysis, estimated that disasters are associated with a 17% increase in the best mean estimate prevalence of psychopathology in comparison to pre-disaster or control group rates. Studies were selected which represented the entire range of disasters and associated psychiatric morbidity, whereas the National Center for PTSD recently released an extensive report that reviews the literature on the 80 different disasters known to have

been examined from a psychiatric perspective since 1981 (Norris et al., 2001). Although Tables 1 and 2 are divided into natural and man-made disasters, it is unclear whether this distinction holds psychiatric relevance. Some studies conclude that man-made disasters induce psychopathology at either greater rates (North and Smith, 1990) or for longer durations (Green and Lindy, 1994; Baum et al., 1983) than natural disasters because victimization by one’s fellow man or women may engender a greater sense of vulnerability. However, the 1991 review by Rubonis and Bickman, in analyzing multiple disaster studies, found that natural disasters were associated with worse psychopathology than were those that were man-made. And, for example, one study found no significant difference in elevated rates of post-traumatic stress disorder (PTSD) among Armenians exposed to either a severe earthquake or severe political violence (Goenjian et al., 2000). In fact, many disasters do not readily lend themselves to the natural vs. man-made dichotomy (Berren et al., 1980). For example, the 1974 Buffalo Creek dam collapse could be attributable to both heavy rains and industrial mismanagement. Ultimately, available information suggests that greater refinement is required in these conceptualizations, possibly taking into account the more specific variables of violence, the predictability and duration of events, and the sense of control over the events (Baum and Davidson, 1986; Biegel and Berren, 1985; Norris et al., 2001). Such an accounting should include measures of not only symptoms but also differences in social and psychological responses to tragedy (Biegel and Berren, 1985). Indeed, disasters are not traumatic psychiatric insults, per se. Many responses to disasters are considered ‘normal’ (Lindemann, 1944). However, there are also major identifiable psychiatric disorders that are amenable to preventive measures and treatment, a discussion of several of which follows. 2.1. Acute stress disorderypost-traumatic stress disorder Acute stress disorder (ASD), as defined in DSM-IV, is detectable 4 days to 4 weeks after a

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Table 1 Natural disasters and their psychiatric sequelae Disaster

Year

Psychiatric morbidity

References

Earthquakes Ecuador

1987

‘Emotional stress’ and physical complaints more in unmarried. Elevated cortisol levels in group of male survivors with high PTSD score and profound lifestyle change. Higher levels of direct exposure, older age, female sex, lower social support correlated with higher psychiatric morbidity. Similar results, despite decline at 2 years’ follow-up. Those with persistent symptoms were more likely to have used psychotropic medication and to have had prior life events. 5-year perspective study: severity of exposure correlated with PTSD, depression, anxiety. Rates were similar 4.5 years later; depression declined, but remained elevated. Effects of high exposure may be reduced by enhanced social supportyassistance.

Lima et al., 1989

Hanshin-Awaji, Japan

1995

Newcastle, Australia

1989

Armenia

1988

North China

1998

Weather related Cyclone, Fiji Islands

1983

Flashfloodsy mudslides, Puerto Rico Hurricane Andrew, South Florida Hurricane Hugo, SC

Hurricane Juan, West Virginia Hurricane Mitch, Nicaragua Volcanoes Mt. Pinatubo, Phillipines Mt. St. Helen, Washington

1985

1992 1989

1985 1998

1991 1980

Affected community had elevated scores on General Health Questionnaire compared to non-affected at 2 months, a difference that normalized at 3 months. High gastrointestinal and pseudoneurological symptoms 1 year later. 36% PTSD, 30% MD, 11% GAD, 10% PD 6–12 months later. 5% of school-aged children meet criteria for PTSD at 3 months, with females and younger children being at higher risk. Family forced to leave town: High levels of PTSD declining by 16 months. High rates of PTSD and MD among adolescents in high versus low exposure cities. 14% major depression and 27.6% PTSD in tribal and non-tribal victims at 6 years. Higher rates of depression, GAD & PTSD correlated with degree of exposure.

Fakuda et al., 2000

Carr et al., 1995 Carr et al., 1997a Carr et al., 1997b

Goenjian et al., 2000

Wang et al., 2000

Fairley et al., 1986

Escobar et al., 1992

David et al., 1996 Shannon et al., 1994

Steinglass and Gerrity, 1990 Goenjian et al., 2001

Howard et al., 1999 Shore et al., 1986

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Table 1 (Continued) Disaster

Year

Psychiatric morbidity

References

Fires South Australia bushfires

1983

14% of firefighters: PTSD 29 mo. post. Victims: PTSD 1-year post. greater in females. Anxiety, dissociative symptoms correlated with direct fire contact, being female & prior stressful life events.

McFarlane, 1986

OaklandyBerkeley, CA

1991

Gregg et al., 1995

Abbreviations: PTSD, posttraumatic stress disorder; GAD, generalized anxiety disorder; MD, major depression; PD, panic disorder.

traumatic event, and includes four major types of symptoms: avoidance, hyperarousal, re-experiencing of events, and (at least three) dissociative symptoms (e.g. sense of numbing, derealization, depersonalization, and dissociative amnesia). In contrast to PTSD, by definition, ASD lasts fewer than 30 days. PTSD consists of at least 30 days of the major symptom clusters of ASD with the exception of dissociation. The severity of the initial ‘acute stress reaction’ in the first 3 months following the traumatic event (as assessed by the Impact of Event Scale) may be predictive of who ultimately develops PTSD (Koren et al., 1999). The diagnosis of ASD predicts PTSD (Classen et al., 1998), and as many as 57–83% of patients with ASD later develop PTSD (Bryant et al., 2000; Brewin et al., 1999). There is some debate as to which, if any, cluster of symptoms or individual symptoms of ASD are the most specific predictors of subsequent PTSD. The extent of dissociative symptoms has been found to correlate with the presence of other posttraumatic stressors and may then predict the future risk of developing PTSD (Eriksson and Lundin, 1996). However, other studies have shown that the re-experiencing, avoidance, and arousal symptom clusters of ASD have greater predictive power for PTSD than does the dissociative symptom cluster (Brewin et al., 1999; Harvey and Bryant, 2000). A substantial proportion of individuals with characteristic PTSD symptoms in the 1st month after trauma may not have experienced significant peritraumatic dissociation and thus would not meet criteria for acute stress disorder (Harvey and Bryant, 1999; Marshall et al., 1999). Thus, the absence of full criteria for ASD, including dissociative symptoms, should not be taken to mean that a

disaster victim is not at risk for development of PTSD. Recently, both a structured interview schedule and a self-report scale for ASD have been developed by Bryant et al. at the University of New South Wales (Bryant et al., 1998a, 2000). Both are highly sensitive for detecting ASD and predicting subsequent PTSD, although we are not aware of reports of their clinical or research use in the acute aftermath of disasters. There exists a wide range of structured instruments available for diagnosing PTSD (Lating et al., 1995; Blake et al., 1995), a full discussion of which is beyond the scope of this review. The recently published study of PTSD and depression in Manhattan in the first 2 months after the September 11 attacks exemplifies how one instrument, the Diagnostic Interview Schedule for PTSD, can be applied acutely (Galea et al., 2002). North et al. (1999) developed the Diagnostic Interview ScheduleyDisaster Supplement, which examines PTSD, seven other psychiatric syndromes, and disaster exposure, and implemented it 6 months after the Oklahoma City bombing in what may be characterized as a sub-acute period. Extension of the research applications of these and other instruments post-disaster to clinical evaluations would appear warranted. 2.2. Other anxiety disorders Among the anxiety disorders other than ASDy PTSD, generalized anxiety disorder (GAD) has been consistently detected following disasters. GAD is distinguished by the presence of multiple worries about a number of events or activities in association with various physical symptoms such

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Table 2 Man-made disasters and their psychiatric sequelae Disaster Technological accidents Chemical exposure (methyl parathion): Mississippi Dam collapse: Buffalo Creek, W. Virginia Nuclear reactor: Three Mile Island, PA

Year

Psychiatric morbidity

References

1996

55% of subjects meet cutoff for clinical depression on self-report instrument, the risk for which correlated with exposure. 14 years later 28% had PTSD & 30% other psychopathology. 35% of community sample of mothers had clinically significant distress at the time of the accident; after remitting, their symptoms recurred with future TMI related events. 6 years later 35.8% had some psychiatric disorder (depression, anxiety). Females 2= males; risk factors include evacuation from home and mother of children less than age 18. Elevated risk for GAD, PTSD, and depression in high exposure vs. low exposure community at 1 year.

Rehner et al., 2000

6 months later, 34.3% have PTSD, of which 74% were new cases and 89% were chronic. Emotional and television exposure correlate with post-traumatic stress symptoms in middle school students at 7 weeks. Prominent post-traumatic sequelae in children in the 1st year and at 4 years; some differences from adult PTSD symptoms. Case reports demonstrate the development and exacerbation of PTSD, major depression, anxiety disorders. PTSD rates 1–2 months post-disaster reach 7.5% in Manhattan overall and 20% in those near the World Trade Center.

North et al., 1999

1972 1979

Nuclear reactor: Chernobyl, USSR

1986

Oil spill: Exxon Valdez, Alaska

1989

Terrorism Oklahoma City, OK

1995

School bus: Chowchilla, CA

1976

World Trade Center

1993

2001

Transportation accidents Airplane: Ramstein AFB

1988

Airplane: Lockerbie, Scotland

1988

Airplane: Boeing 737 Kegsworth, UK Airplane: cargo crash into apartment bldg., Netherlands Boat: Belgium

1989 1992

1987

PTSD 18 months later correlated with level of education, exposure to burn injury, numbness during crash, stressful life events post. 44% PTSD in insurance claimants seen at 10–14 months; depression next most common diagnosis; no significant predictors of diagnosis or severity. 40% PTSD in survivors 6–12 months post. 26% survivors had PTSD—correlated with loss of loved one, home at time, loss of home. At 6 and 30 months, elevated rates of alcohol use correlate with psychological

Green et al., 1990 Dew and Bromet, 1993

Havenaar et al., 1996

Palinkas et al., 1993

Pfefferbaum et al., 2001

Terr, 1981, 1983

Difede et al., 1997

Galea et al., 2002

Epstein et al., 1998

Terr, 1981

Gregg et al., 1995 Carlier and Gersons, 1997

Joseph et al., 1993

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Table 2 (Continued) Disaster

Year

Boat: Athens

1988

Subway station: London, UK

1987

School bus: Western Norway

1989

Psychiatric morbidity distress Better mental outcome correlated with higher perceived crisis support Psychopathology associated with prior problems & subsequent stressful life events and social disruption General psychiatric symptoms elevated 5 years later in parents and spouses

References Joseph et al., 1992 Rosser et al., 1991

Winje, 1996

Abbreviations: PTSD, post-traumatic stress disorder; GAD, generalized anxiety disorder; MD, major depression; PD, panic disorder; TMI, Three-Mile Island.

as restlessness and muscle tension. It has been described as long as 6 years after the Chernobyl nuclear accident (Havenaar et al., 1996), 3–4 years after the Mount St. Helens explosion (Shore et al., 1986), 1 year after the Exxon Valdez oil spill (Palinkas et al., 1993), and 6–12 months after Hurricane Andrew (David et al., 1996). Hurricane Andrew was also associated with an increased incidence of panic disorder. 2.3. Major depression A genetic predisposition for major depression increases the risk for a major depressive episode (MDE) following a stressful life event (Kendler et al., 1995, 1998). After a jet fighter accidentally crashed into an Indianapolis hotel, all survivors with a prior history of major depression developed an MDE (Smith et al., 1990). More severe prior life events and a greater number of such events also influence the likelihood of developing an MDE after a trauma (Kendler et al., 1998), although one study found that post-disaster, rather than pre-disaster, life events alone correlated with the avoidant-depressive symptomatology of PTSD (Maes et al., 2001). Those with greater exposure to the Mount St. Helens volcanic eruption had higher rates of major depression than those with lower exposure (Shore et al., 1986). Whether an individual has had other recent life difficulties and the nature of the available social supports also have some effect on the development of an MDE (Kendler et al., 1993). Thus, severity of exposure to the disaster, a family or personal history of MDE, the presence

of outside stressors, and availability of social supports all appear to be factors that contribute to the risk of development of MDE following a trauma. The first 3 months after stressful life events pose the greatest risk period for onset of an MDE (Surtees et al., 1986; Kendler et al., 1993, 1995, 1998). Thus, the extended presence of a mental health professional immediately after a disaster could aid in the detection, and possibly the mitigation, of serious depressive episodes. Clinicianadministered and self-administered depression inventories for the purpose of efficiently detecting MDE have been developed by previous researchers (Beck et al., 1961; Hamilton, 1960). 2.4. Psychosis Little is documented about the incidence of psychosis following disasters, and research about the effects of disasters on psychotic patients is scant. Such an effect might be predicted based on known associations between stressful life events and the acute onset or relapse of schizophrenia (Corcoran et al., 2002). One study reported that the rates of hospital admissions for newly diagnosed schizophrenia increased in Lebanon during the periods of intense civil war in the 1970s and 1980s compared to pre-war rates (Yatkin and Labban, 1992). In the 4-month period following the fall of the Berlin Wall, patients with schizoaffective disorder were found to have longer and more severe recurrences when compared to the same period in the prior year (Bohlken and Priebe, 1991). In contrast, the existing, largely un-controlled studies of hospitalized patients with pre-

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existing schizophrenia suggest that these patients do not decompensate in the wake of disasters but may actually maintain a higher level of functioning (Edwards, 1976; Godleski et al., 1994; Chubb and Bisson, 1996; Koegler and Hicks, 1972; McMurray and Steiner, 2000). 2.5. Substance use disorders Despite clinical observations of an association between substance abuseydependence and disasters and the high rates of co-morbidity between alcohol and drug abuse and PTSD (Acierno et al., 1999; Kosten et al., 2000), only a few studies have addressed this issue. Four to six weeks after the accidental crash of a military jet into a hotel, only half of those who were abusing alcohol prior to the incident were still abusing it and only 4% of all subjects developed a new alcohol use disorder (Smith et al., 1990). Following the Oklahoma City bombing, the majority of predisaster alcohol and drug use disorders were reported as quiescent and no new disorders were detected (North et al., 1999). On the other hand, 49% of survivors of a 1987 ferry accident near Belgium self-reported that their alcohol consumption increased ‘a lot’ in the 6 months after the accident (Joseph et al., 1993). 3. Predictors of later psychiatric illness 3.1. Biological predictors A distinct biological response appears to underlie abnormal responses to trauma and distinguishes them from normal responses (Yehuda and McFarlane, 1995). Reduced urinary cortisol in trauma victims who go on to develop PTSD suggests that traumatic events are biologically distinguishable from stressful events (Yehuda, 1997, 2000; Yehuda and McFarlane, 1995). Whereas normal stressful responses produce an elevated cortisol response, abnormal responses exhibit the opposite (Yehuda, 2000). Norepinephrine has been thought to play an important role in consolidating memories of emotional or stressful events (Southwick et al., 1999), and evidence of an overactive noradrenergic sys-

207

tem has also been implicated in abnormal responses to stress (Yehuda, 2000; Southwick, et al., 1997). PTSD sufferers, when compared to those without PTSD, have been noted to have heightened heart rates and blood pressures in the peri-trauma period, elevations of these same parameters upon re-exposure to trauma-related stressors, elevated urinary catecholamines, and a sensitivity to develop panic attacks when given yohimbine, which enhances adrenergic tone (Southwick et al., 1997). Taken together, these findings suggest that individuals who exhibit the combination of a reduced cortisol response and a heightened adrenergic response to trauma may be especially likely to develop PTSD in the wake of traumas, including disasters (Yehuda, 2000). It is unclear whether these deviations constitute a pre-trauma vulnerability or an effect of the trauma itself. Shalev (2000), in a comprehensive review of the psychobiological responses to disasters, has nonetheless suggested that this potential interaction of the glucocorticoid and adrenergic systems, as well as the separate impact of secondary stresses and interpersonal losses on the glucocorticoid system, may together provide the biological substrate for psychopathology in the period following a disaster. Thus, following a disaster, blunted cortisol levels and increased adrenergic tone could potentially serve as factors that (a) permit modification by psychiatric interventions and (b) serve as biological markers of those at risk for future psychopathology. 3.2. Demographic predictors In addition to symptoms of ASD, preexisting psychiatric history is an important predictor of the likelihood of developing PTSD (North et al., 1994; Schnurr et al., 1993; Helzer et al., 1987; Bremner et al., 1993; Zaidi and Foy, 1994; Resnick et al., 1992). In a study by Smith et al. (1990), 90% of subjects with a pre-disaster psychiatric diagnosis went on to have post-disaster pathology, whereas 25% of subjects without such a history developed post-disaster psychiatric pathology (where the preand post disaster psychiatric disorders under investigation were alcohol abuseydependence, clinical

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depression, PTSD or GAD). A previous history of depression may, in particular, increase the risk of developing PTSD (Shalev et al., 1998b) and depression manifesting within the first month after a trauma itself constitutes a strong predictor of PTSD 1 year later (Freedman et al., 1999). Beyond the presence of a prior psychiatric history, perhaps one of the most replicated findings in the literature has been the direct correlation between severity (or ‘dose’) of exposure to a disaster and the likelihood of development of PTSD (Green and Lindy, 1994; Carr et al., 1997a,b; Lima et al., 1989; Shore et al., 1986; Basoglu et al., 1994; Goenjian et al., 2000), regardless of whether dose of exposure was defined by proximity to the disaster (Lima et al., 1989; Goenjian et al., 2000), subjective report (Carr et al., 1997a,b; Basoglu et al., 1994), the number of lives lost or the extent of property damaged (Shore et al., 1986). Importantly, though, it is not necessary to have high traumatic exposure to be at risk for developing PTSD, as is illustrated by a study of bystanders to a shootout, who never saw the gunman or the victims, yet still went on to develop ASD and PTSD (Classen et al., 1998). However, one study of earthquake survivors in North China found higher rates of PTSD in a village at a greater distance from an earthquake epicenter than a closer comparison group (Wang et al., 2000). Importantly, however, the more highly exposed village was found to have received greater social supports from government and nongovernment agencies. Other studies have likewise highlighted the considerable role that psychosocial supports play in modulating the psychological impact of a disaster (Lewin et al., 1998; Lima et al., 1989; Dew and Bromet, 1993; Carr et al., 1997a,b). These findings extend beyond survivors of earthquakes (Lewin et al., 1998; Lima et al., 1989; Dew and Bromet, 1993; Carr et al., 1997a,b) to survivors of torture (Basoglu et al., 1994) and relief workers themselves (Epstein et al., 1998) and appear to include both pre-disaster and postdisaster personal problems that may be unrelated to the event itself. However, one study did find that post-disaster life events, but not those which preceded the disaster, predicted rates and severity of PTSD (Maes et al., 2001). Studies that have

defined ‘dose’ of disaster exposure in terms of lives lost may also be indirectly measuring a disaster-induced diminution in the level of social support. Female sex has been frequently found to be a risk factor for post-traumatic and post-disaster psychiatric morbidity, including PTSD (North et al., 1999; Norris et al., 2001). However, this has not always been replicated (Gregg et al., 1995) and some researchers have questioned whether women indeed have a differential vulnerability to trauma (Yehuda, 2002). In addition, a recent review suggests that both minority and lower socioeconomic status may also be risk factors for post-disaster psychopathology (Norris et al., 2001), although these may be related to the broader role of pre- and post-disaster psychosocial problems. 4. Acute psychiatric interventions The desire to minimize the long-term psychiatric consequences of disasters has led the US Navy to form Special Psychiatric Intervention Teams (SPRINT) and the US Army to form a Stress Management Team (SMT). However, publications about these teams appear to assume that their interventions will prevent psychiatric morbidity without containing supporting data (McCaughey, 1987; Sokol, 1989), while others have acknowledged that acute interventions are often performed post-trauma on the basis of good intentions and theorized benefits (Lundin, 1994; Duckworth, 1991). The following section examines the data that presently exist in support of acute psychiatric interventions subsequent to a disaster (see Table 3). 4.1. Debriefing Debriefings have been defined as group discussions that occur within 48–72 h after an event and are often referred to as ‘psychological de-briefings’ (Bisson and Deahl, 1994; Shalev et al., 1998a). In general, these sessions encourage participants (usually emergency workers) to describe and share both factual and emotional aspects of their disaster experience. The widespread use of this modality

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Table 3 Overview of research on acute psychiatric interventions at disaster sites Intervention Psychopharmacology Benzodiazepines

Anti-depressants b-Adrenergic blockers Glucocorticoids Other modalities EMDR Individual psychotherapy

Summary of findings

References

Conflicting findings regarding their ability to mitigate or prevent ASDyPTSD; uncertain benefit for chronic PTSD Imipramine may treat ASD; citalopram could prevent PTSD Propranolol reduces memories of traumatic videos in healthy volunteers Hydrocortisone reduced rates of PTSD in sepsis patients versus controls

Gelpin et al., 1996; Braun et al., 1990; Kosten et al., 2000

No current evidence supports its use with disaster victims CBT and prolonged exposure therapy may treat or prevent ASDyPTSD, consistent with studies in chronic PTSD

Shapiro, 1989a,b; Lohr et al., 1995, 1999 Pitman et al., 1996; Grainger et al., 1997 Frank et al., 1988; Foa et al., 1995 Difede et al., 1997; Bryant et al., 1998a,b Bryant et al., 1999; Marks et al., 1998 Tarrier et al., 1999 Herman and Schatzow, 1984; Hazzard et al., 1993 Lubin et al., 1998; Dembert and Simmer, 2000 Bisson and Deahl, 1994; Deahl et al., 1994 Hobbs et al., 1996; Van der Kolk, 1997 Shalev et al., 1998a; Chemtob et al., 1997 Rose et al., 1999; Kaplan et al., 2001 Goenjian et al., 1997; Chemtob et al., 2002

Group psychotherapy Some evidence in rape victims suggests that different group modalities may treat PTSD Debriefing Possible evidence from non-randomized trials to support its use; no randomized trials support its use post-trauma; lack of trials post-disaster Child psychotherapy Some evidence from controlled studies that group or individual psychotherapy programs reduce PTSD in children and adolescents 1–3 years post-disaster

Blaha et al., 1999; Robert et al., 1999 Cahill et al., 1994; Van Stegeren et al., 1998 Schelling et al., 1999

Abbreviations: ASD, acute stress disorder; CBT, cognitive-behavioral therapy; PTSD, post-traumatic stress disorder; EMDR, eye movement desensitization and reprocessing.

in disaster settings derives from the belief that immediate processing gives an individual the ability to cognitively restructure the event so that it is remembered in a less traumatic way. The cognitive restructuring is thought to involve a switching from a non-verbal sensory form of memory to a verbal or semantic memory (reviewed in Van der Kolk, 1997). Consistent with this interpretation is a preliminary report by Rauch et al. (1996) using positron emission tomography (PET) in patients with PTSD. Subjects were exposed to detailed narratives of their own trauma and then observed by PET to activate right hemisphere, amygdala, surrounding temporal lobe, and right visual cortex, but decreased activity was observed in the left

inferior frontal region corresponding to Broca’s area. Although this study was not a longitudinal examination of trauma victims before and after debriefing, it nevertheless suggests that individuals who develop PTSD may not be able to respond verbally to the emotional reaction produced after a traumatic event. Thus, it follows that debriefing by encouraging verbalization, could aid in defusing the strongly right-sided and potentially pathological temporal lobe and limbic system response and in doing so possibly prevent PTSD. However, debriefing is controversial. While some studies do suggest it is beneficial, others suggest it may actually produce harm. Shalev et al. (1998a) found that soldiers’ pre-intervention anxiety as well as self-estimation of their ability

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to function in combat significantly improved immediately after undergoing a debriefing within 72 h of a combat situation. Other authors have found that debriefings done at either 6 or 9 months after exposure to a hurricane led to significant reductions in scores on the Impact of Event Scale 3 months post-intervention (Chemtob et al., 1997). Neither of these studies was controlled, although the latter attempted to control for the passage of time. With regard to controlled studies, in a naturalistic study of emergency personnel who did or did not undergo debriefing following an earthquake, investigators found that the debriefed group reported finding the sessions ‘very’ or ‘somewhat’ helpful, although the actual development of post-traumatic stress and other psychological symptoms was unaffected by the intervention (Kenardy et al., 1996). The authors pointed out that the study was limited by their inability to standardize the intervention. In a naturalistic study of Gulf War veterans, Deahl et al. (1994) likewise found a lack of effect of debriefing on subsequent psychiatric morbidity. Two randomized controlled studies of debriefing in victims of violent crime (Rose et al., 1999) and auto accidents (Hobbs et al., 1996) failed to find any benefit when subjects were assessed for post-traumatic symptomatology several months after undergoing debriefings. The latter study even suggested a possible worsening of symptoms in the treatment group. Indeed, in another randomized, controlled study of burn victims who underwent a modified form of debriefing within 2–19 days of the trauma, individuals exposed to debriefings had a higher incidence of PTSD than did controls (Bisson et al., 1997). These contradictory results call into question the utility of debriefing and have led some to suggest that it should be discontinued until further rigorously controlled research provides evidence for its efficacy (Wessely et al., 2000). At the very least, further evidence from controlled studies is required to support the use of debriefing after trauma (Kaplan et al., 2001). And certainly it would be important to conduct controlled studies on the use of debriefings in the wake of disasters in particular.

4.2. Pharmacotherapy The use of psychotropic medications at the time of an acute trauma continues to be considered not good psychiatric practice, on the assumption that they will adversely interact with the individual’s psychological processing of the event (Lundin, 1994). However, this is not supported by any data. In fact, there is a relative scarcity of research on acute medication management for trauma and disaster victims. Gelpin et al. (1996) found no difference in PTSD or anxiety scores in subjects at 1 and 6 months following treatment with a benzodiazepine or placebo. There are no other controlled trials reported with this class of medication in the acute post-disaster setting. Benzodiazepines have been studied for chronic PTSD associated with various traumas, however; Kosten et al. (2000) found that among veterans with PTSD and co-morbid substance abuse problems, the prescription of benzodiazepines did not worsen their condition, did not lead to heightened violence, and was associated with reduced outpatient visits. A controlled study of alprazolam treatment of patients with PTSD 0.67 to 13 years after their traumatic event indicated that the medication may have improved some anxiety symptoms but not specific PTSD symptoms (Braun et al., 1990). Tricyclic antidepressants have been found to be effective in the treatment of symptoms of chronic (i.e. lasting 3 months or longer) PTSD (Marshall and Pierce, 2000). They have also been used in ASD. In an open trial, 25 children admitted to an acute burn unit and who had concurrent ASD were given imipramine at either the dose at which they improved or a dose that gave a therapeutic serum level (Robert et al., 1999). After 4 days of treatment, 80% of the subjects showed no further ASD symptoms and another 12% showed reduced symptoms. In another study, 15 acute burn victims were given the selective serotonin uptake inhibitor citalopram daily for 6 months (Blaha et al., 1999). Not only were they found to have improved wound healing, but also none developed PTSD compared to 50% of untreated controls. No other studies of the acute use of antidepressants have been published.

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Based on the role of dysregulated adrenergic tone in the development of PTSD (Southwick et al., 1997), anti-adrenergic agents have been considered in the prevention and treatment of traumarelated psychopathology. However, only two studies have been reported, and these are in nonclinical samples (Cahill et al., 1994; Van Stegeren et al., 1998). In the first study (Cahill et al., 1994), placebo or the b-blocking agent, propranolol, was given to healthy volunteers 1 h before they were shown either a neutral or an emotional video presentation. Tests of subjects’ memories of the videos 1 week later revealed that propranolol significantly impaired memory of the arousing video separate from its effect on their emotional response but did not affect memory for the neutral video. In a subsequent study using the same paradigm, propranolol was compared to the less centrally acting b-blocking agent, nadolol (Van Stegeren et al., 1998). Propranolol, but not nadolol, impaired memory for the emotional video but not the neutral one. These results suggest a prophylactic role for propranolol in the management of trauma-related psychopathology. With regard to the possible role of glucocorticoids in the pathophysiology of PTSD (Yehuda, 1997, 2000; Yehuda and McFarlane, 1995), one group studied the effect of hydrocortisone on the subsequent development of PTSD among patients being treated in intensive care for septic shock (Schelling et al., 1999). In their retrospective analysis of patients being administered hydrocortisone for hemodynamic reasons, the authors found a significantly lower rate of subsequent PTSD when compared with those patients who did not receive this treatment during their treatment for sepsis. No other studies have been published associating glucocorticoid treatment with PTSD outcome. 4.3. Eye movement reprocessing

desensitization

and

Eye movement desensitization and reprocessing (EMDR) is a technique in which traumatized individuals perform saccadic eye movements under the guidance of a therapist while focusing on mental images of the traumatic event. Shapiro,

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who developed this technique, has reported that a single session can successfully help trauma victims to become desensitized from troubling memories and alter their responses to memories of the event (Shapiro, 1989a,b). The technique has since been subject to heavy criticism (Lohr et al., 1999). In particular, its scientific basis is questionable, given that eye movements appear to be incidental to the benefits that may derive from the prolonged image exposure required by EMDR (Lohr et al., 1995). In addition, EMDR has not been done in the immediate aftermath of a traumatic event or disaster (Grainger et al., 1997). 4.4. Individual psychotherapy Although various psychotherapeutic approaches for the treatment of acute trauma have been described (Sokol, 1989; Osterman and Chemtob, 1999; Chertoff, 1998), only cognitive-behavioral therapy has been subjected to rigorous study. Frank et al. (1988) compared cognitive-behavioral therapy (CBT) with systematic desensitization among both immediate (20.1"9.7 days) and delayed (128.7"77.7 days) treatment-seeking rape victims. Both 14-week interventions were associated with improvement in various measures of psychopathology to a level comparable to non-victim controls. Significantly more members of a group of recent rape victims who were treated with a 4-week program of education and CBT recovered from PTSD at 2 months than did controls, although this difference disappeared at 5 months (Foa et al., 1995). Bryant et al. (1998b) similarly found that victims of either motor vehicle or industrial accidents who were treated within 2 weeks of their trauma for ASD with 5 weekly sessions of CBT developed significantly less PTSD 6 months later when compared with other such victims who were given only supportive therapy. Case reports likewise indicate the efficacy of CBT in treating PTSD following the World Trade Center bombing in 1993 (Difede et al., 1997). Prolonged exposure therapy, which involves attention to trauma-related memories and images, has also been found to reduce the onset of PTSD in trauma victims with ASD (Bryant et al., 1999). These acute studies are

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consistent with studies of chronic PTSD, in which both cognitive therapy and imaginal exposure have been found to be effective but not significantly different from each other in their impact (Marks et al., 1998; Tarrier et al., 1999). 4.5. Group psychotherapy There exist a number of studies that have examined the use of various types of group psychotherapy for women who have suffered sexual abuse or other traumas (Herman and Schatzow, 1984; Hazzard et al., 1993; Lubin et al., 1998). The approaches used include cognitive-behavioral, process-oriented, and time-limited group therapies. Although various forms of group therapy show promise for the treatment of PTSD and other psychopathology, the lack of male subjects limits the generalizability of these studies to acute disaster work. As they are targeted towards the treatment of existing psychopathology, they also do not address prevention of such problems. Dembert and Simmer (2000) have reviewed the literature on, and their experience with, group interventions with both men and women at various types of disasters. However, there are no studies that addressed the use of group therapy after disasters in anything other than a descriptive fashion. 4.6. Treatment strategies for children The topic of child mental health needs in the wake of disasters represents a broad area to which this article can only brief allude, as reflected in studies following Hurricane Hugo (Shannon et al., 1994), Hurricane Mitch (Goenjian et al., 2001) and the Chowchilla bus kidnapping (Terr, 1981, 1983). A number of immediate psychotherapeutic interventions on both the group and individual level have been described, including a public health model that employs both age-appropriate trauma-narrative work and a range of social environmental interventions (Pynoos et al., 1998), and some of these have undergone empirical evaluation. Chemtob et al. (2002) reported a significant reduction in trauma-related symptoms in schoolaged children who underwent a four-session man-

ualized group or individual psychotherapy program involving art, play therapy, and talk 2 years after Hurricane Iniki. One and one half years after the 1988 Armenian earthquake, young adolescents who received trauma and grief-focused psychotherapy had a reduction in PTSD symptoms that was significantly different from controls (Goenjian et al., 1997). 5. Conclusion Regardless of the specific type, disasters may lead to psychiatric morbidity. This morbidity is well established in long-term follow-up studies. There exist a number of risk factors for eventual psychiatric sequelae that may assist psychiatrists in identifying victims who require follow-up beyond the acute event. A scant but suggestive literature points to the possibility that psychotropic medications, if administered acutely, could prevent some psychiatric morbidity. In addition, literature on non-somatic interventions for trauma and disaster victims suggests that cognitive-behavioral and group psychotherapy may offer some additional benefit in the acute disaster period. The roles of both debriefing and EMDR remain uncertain. Our review reveals the need for more extensive research into the prevention and treatment of psychiatric sequelae of disasters. Viewing disasters as multi-dimensional events, of which one facet is psychiatric, may help to ease unnecessary suffering and dysfunction both as victims try to overcome the immediate social, political, and economic obstacles to restoring normality to their lives, and as the ‘dust settles’ in the future and these victims try to finally return to their old lives. Early psychiatric intervention appears crucial to halt progressive long-term debilitation. Disasters are unique among the traumas in their very public nature, making them perhaps uncommonly accessible for the sake of treating and studying traumas. Unfortunately much-needed controlled treatment and preventative trials at the time of a disastrous event are practically difficult to implement. As we witnessed in the aftermath of the horrific events of September 11, 2001, any prospective research becomes secondary to the crucial clinical efforts of psychiatrists and, with the exception of recorded

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retrospective clinical observations, has not been possible without Institutional Review Board approval that at most academic centers takes a minimum of a few weeks or months. Thus, the necessary timeliness of such research will unfortunately need to be considered now for implementation during a future disaster. We would suggest that an important first step in this process be the inclusion of a mental health screening protocol in the disaster planning of some localities or agencies. This protocol could help to identify mental health ‘casesness’ among disaster victimsysurvivors by means of a screening instrument. This would be followed by a clinical interview to assess the clinical needs of those identified by the instrument, thereby serving a crucial clinical function while simultaneously assessing the validity of the instrument in the acute setting of a disaster. The General Health Questionnaire, a brief self-report measure of general mental health that may also be predictive of PTSD (Goldberg and Hillier, 1979), has been used in a number of disaster research studies cited in this article and thus may be ideal for these purposes (Gregg et al., 1995; McFarlane, 1986; McFarlane et al., 1997). Such an arrangement would require approval from a number of agencies, including an institutional review board and either private or government relief agencies such as the Red Cross or the Federal Emergency Management Agency. Only through learning how to identify people with acute mental health needs post-disaster can we can go on to conduct more rigorous intervention trials with them. Acknowledgments Funding from the Langeloth Foundation and Pfizer, Inc., has been provided to the charitable organization, Disaster Psychiatry Outreach. C.L.K. is grateful to Dr Rachel Yehuda for her guidance in the preparation of this article. References Acierno, R., Kilpatrick, D.G., Resnick, H.S., 1999. Posttraumatic stress disorder in adults relative to criminal victimization: prevalence, risk factors, and comorbidity. In: Saigh,

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